Cited by 310Tryptophan and brain disordersVagus Nerve Stimulation ResearchStress Responses and Cortisol

Stress, Food, and Inflammation: Psychoneuroimmunology and Nutrition at the Cutting Edge

Open access
Kiecolt-Glaser, Janice K.·2010·Psychosomatic Medicine

Abstract

Inflammation is the common link among the leading causes of death. Mechanistic studies have shown how various dietary components can modulate key pathways to inflammation, including sympathetic activity, oxidative stress, transcription factor nuclear factor-kappaB activation, and proinflammatory cytokine production. Behavioral studies have demonstrated that stressful events and depression can also influence inflammation through these same processes. If the joint contributions of diet and behavior to inflammation were simply additive, they would be important. However, several far more intriguing interactive possibilities are discussed: stress influences food choices; stress can enhance maladaptive metabolic responses to unhealthy meals; and diet can affect mood as well as proinflammatory responses to stressors. Furthermore, because the vagus nerve innervates tissues involved in the digestion, absorption, and metabolism of nutrients, vagal activation can directly and profoundly influence metabolic responses to food, as well as inflammation; in turn, both depression and stress have well-documented negative effects on vagal activation, contributing to the lively interplay between the brain and the gut. As one example, omega-3 fatty acid intake can boost mood and vagal tone, dampen nuclear factor-kappaB activation and responses to endotoxin, and modulate the magnitude of inflammatory responses to stressors. A better understanding of how stressors, negative emotions, and unhealthy meals work together to enhance inflammation will benefit behavioral and nutritional research, as well as the broader biomedical community.

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Registry

Crossref · 10.1097/psy.0b013e3181dbf489

Cites

61 of 61 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

0 of 44 cited sources checked · 0 supported · 0 flagged

  • Premisecitation

    Stress and depression can directly provoke proinflammatory cytokine production without infection or injury.

    “stress and depression can also directly provoke proinflammatory cytokine production in the absence of infection or injury (17-18).”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [17] Kiecolt-Glaser JK McGuire L Robles TR Glaser R Emotions, morbidity, and mortality: New perspectives from psychoneuroimmunology Annu Rev Psychol 2002 53 83 107 11752480 source

      Not checked in the free run.

    • cites [18] Howren MB Lamkin DM Suls J Associations of depression with C-reactive protein, IL-1, and IL-6: A meta-analysis Psychosom Med 2009 71 171 86 19188531 source

      Not checked in the free run.

  • Premisecitation

    Stress can worsen maladaptive metabolic responses to unhealthy meals.

    “stress can enhance maladaptive metabolic responses to unhealthy meals”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [50] Le Fur C Romon M Lebel P Devos P Lancry A Guedon-Moreau L Fruchart JC Dallongeville J Influence of mental stress and circadian cycle on pastprandial lipemia Am J Clin Nutr 1999 70 213 20 10426697 source

      Not checked in the free run.

    • cites [51] Stoney CM West SG Hughes JW Lentino LM Finney ML Falko J Bausserman L Acute psychological stress reduces plasma triglyceride clearance Psychophysiology 2002 39 80 5 12206298 source

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  • Premisecitation

    NF-κB is a key bridge for stress-induced increases in proinflammatory cytokines and their genes.

    “NF-κB appears to be a prime bridge for stress-induced increases in proinflammatory cytokines and the genes that control their expression (5).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [5] Bierhaus A Wolf J Andrassy M Rohleder N Humpert PM Petrov D Ferstl R von Eynatten M Wendt T Rudofsky G Joswig M Morcos M Schwaninger M McEwen B Kirschbaum C Nawroth PP A mechanism converting psychosocial stress into mononuclear cell activation Proc Natl Acad Sci U S A 2003 100 1920 5 12578963 PMC149934 source

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  • Premisecitation

    Inflammation is implicated in the pathophysiology of depression.

    “Several lines of research have implicated inflammation in the pathophysiology of depression (13-14).”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [13] Miller GE Backwell E Turning up the heat: Inflammation as a mechanism linking chronic stress, depression, and heart disease Curr Dir Psychol Sci 2006 15 269 72 source

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    • cites [14] Raison CL Capuron L Miller AH Cytokines sing the blues: Inflammation and the pathogenesis of depression Trends Immunol 2006 27 24 31 16316783 PMC3392963 source

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  • Premisecitation

    Stressful events and depression can influence inflammation through the same pathways as diet.

    “Behavioral studies have demonstrated that stressful events and depression can also influence inflammation through these same processes.”
    Quote in the paperSubstantial claim0 of 3 sources checked
    • cites [5] Bierhaus A Wolf J Andrassy M Rohleder N Humpert PM Petrov D Ferstl R von Eynatten M Wendt T Rudofsky G Joswig M Morcos M Schwaninger M McEwen B Kirschbaum C Nawroth PP A mechanism converting psychosocial stress into mononuclear cell activation Proc Natl Acad Sci U S A 2003 100 1920 5 12578963 PMC149934 source

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    • cites [6] Epel ES Blackburn EH Lin J Dhabhar FS Adler NE Morrow JD Cawthon RM Accelerated telomere shortening in response to life stress see comment Proc Natl Acad Sci U S A 2004 101 17312 5 15574496 PMC534658

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    • cites [7] Steptoe A Hamer M Chida Y The effects of acute psychological stress on circulating inflammatory factors in humans: A review and meta-analysis Brain Behavior and Immunity 2007 21 901 12 17475444 source

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  • May combine two claims. 10
  • May combine two claims.

    Interpretationcitation

    Diet can affect mood and the magnitude of inflammatory responses to stressors.

    “diet can impact mood as well as proinflammatory responses to stressors”
    • Also stated in: § Dietary Influences on Mood and Proinflammatory Stress Responses: Omega-3 and Omega-6 · hedged
      “these studies (26, 28) suggest that diet can influence the magnitude of inflammatory responses to stress and depression as well as mood.”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [26] Maes M Christophe A Bosmans E Lin AH Neels H In humans, serum polyunsaturated fatty acid levels predict the response of proinflammatory cytokines to psychologic stress Biol Psychiatry 2000 47 910 20 10807964 source

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    • cites [28] Kiecolt-Glaser JK Belury MA Porter K Beversdorf D Lemeshow S Glaser R Depressive symptoms, omega-6:omega-3 fatty acids, and inflammation in older adults Psychosom Med 2007 69 217 24 17401057 PMC2856352 source

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  • May combine two claims.

    Premisecitation

    Depression and stress reduce vagal activation.

    “both depression and stress have well-documented negative effects on vagal activation”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [52] Yin J Levanon D Chen JDZ Inhibitory effects of stress on postprandial gastric myoelectrical activity and vagal tone in healthy subjects Neurogastroenterol Motil 2004 16 737 44 15601423 source

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    • cites [54] Pieper S Brosschot JF van der Leeden R Thayer JF Cardiac effects of momentary assessed worry episodes and stressful events Psychosom Med 2007 69 901 9 17991822 source

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    Premisecitation

    Omega-3 fatty acid intake dampens NF-κB activation and endotoxin responses.

    “dampen NF-κB activation and responses to endotoxin”
    Quote in the paperSubstantial claim0 of 4 sources checked
    • cites [32] Zhao Y Joshi-Barve S Barve S Chen LH Eicosapentaenoic acid prevents LPS-induced TNF-alpha expression by preventing NF-kappaB activation J Am Coll Nutr 2004 23 71 8 14963056 source

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    • cites [33] Jolly CA Muthukumar A Avula CP Troyer D Fernandes G Life span is prolonged in food-restricted autoimmune-prone (NZB × NZW)F(1) mice fed a diet enriched with (n-3) fatty acids J Nutr 2001 131 2753 60 11584100 source

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    • cites [39] Michaeli B Berger MM Revelly JP Tappy L Chiolero R Effects of fish oil on the neuro-endocrine responses to an endotoxin challenge in healthy volunteers Clinical Nutrition (Edinburgh, Scotland) 2007 26 70 7 17055120 source

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    • cites [40] Pluess TT Hayoz D Berger MM Tappy L Revelly JP Michaeli B Carpentier YA Chiolero RL Intravenous fish oil blunts the physiological response to endotoxin in healthy subjects Intensive Care Med 2007 33 789 97 17377770 source

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  • May combine two claims.

    Premisecitation

    Diets that promote inflammation are high in refined starches, sugar, saturated and trans fats, and low in omega-3 fatty acids, antioxidants, and fiber.

    “Diets that promote inflammation are high in refined starches, sugar, saturated and trans-fats, and low in omega-3 fatty acids, natural antioxidants and fiber from fruits, vegetables, and whole grains (1).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [1] Giugliano D Ceriello A Esposito K The effects of diet on inflammation - Emphasis on the metabolic syndrome J Am Coll Cardiol 2006 48 677 85 16904534 source

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  • May combine two claims.

    Premisecitation

    Chronic stressors increase IL-6 and oxidative stress.

    “the average annual rate of increase in serum IL-6 was about four times as large in men and women who were chronically stressed by caregiving for a spouse with dementia compared to similar individuals with no caregiving responsibilities (23).”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [23] Kiecolt-Glaser JK Preacher KJ MacCallum RC Atkinson C Malarkey WB Glaser R Chronic stress and age-related increases in the proinflammatory cytokine IL-6 Proc Natl Acad Sci U S A 2003 100 9090 5 12840146 PMC166443 source

      Not checked in the free run.

    • cites [6] Epel ES Blackburn EH Lin J Dhabhar FS Adler NE Morrow JD Cawthon RM Accelerated telomere shortening in response to life stress see comment Proc Natl Acad Sci U S A 2004 101 17312 5 15574496 PMC534658

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Stress increases postprandial lipemia and delays triglyceride clearance.

    “Importantly, stress both enhances post-meal peaks and delays clearance.”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [50] Le Fur C Romon M Lebel P Devos P Lancry A Guedon-Moreau L Fruchart JC Dallongeville J Influence of mental stress and circadian cycle on pastprandial lipemia Am J Clin Nutr 1999 70 213 20 10426697 source

      Not checked in the free run.

    • cites [51] Stoney CM West SG Hughes JW Lentino LM Finney ML Falko J Bausserman L Acute psychological stress reduces plasma triglyceride clearance Psychophysiology 2002 39 80 5 12206298 source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    High-fat meals can cause low-grade endotoxemia and NF-κB activation in PBMCs.

    “High-fat meals can stimulate low-grade endotoxemia”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [36] Erridge C Attina T Spickett CM Webb DJ A high-fat meal induces low-grade endotoxemia: evidence of a novel mechanism of postprandial inflammation Am J Clin Nutr 2007 86 1286 92 17991637 source

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    • cites [37] Blanco-Colio LM Valderrama M Alvarez-Sala LA Bustos C Ortego M Hernandez-Presa MA Cancelas P Gomez-Gerique J Millan J Egido J Red wine intake prevents nuclear factor-kappa B activation in peripheral blood mononuclear cells of healthy volunteers during postprandial lipemia Circulation 2000 102 1020 6 10961967 source

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    Premisecitation

    Fasting protects normal cells but not tumor cells from high-dose chemotherapy.

    “in normal cells, fasting slows the cell cycle and thus is protective. However, tumor cells do not respond to starvation by slowing cell division, and their continued high replicative rate makes them more vulnerable to chemotherapy (57).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [57] Raffaghello L Lee C Safdie FM Wei M Madia F Bianchi G Longo VD Starvation-dependent differential stress resistance protects normal but not cancer cells against high-dose chemotherapy Proceedings of the National Academy of Sciences 2008 105 8215 20 PMC2448817 18378900 source

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  • May combine two claims.

    Premisecitation

    Omega-3 PUFAs reduce proinflammatory cytokine production and oxidative stress.

    “higher levels of n-3 PUFAs as well as lower n-6:n-3 ratios are associated with lower proinflammatory cytokine production (29).”
    Quote in the paperSubstantial claim0 of 3 sources checked
    • cites [29] Ferrucci L Cherubini A Bandinelli S Bartali B Corsi A Lauretani F Martin A Andres-Lacueva C Senin U Guralnik JM Relationship of plasma polyunsaturated fatty acids to circulating inflammatory markers J Clin Endocrinol Metab 2006 91 439 46 16234304 source

      Not checked in the free run.

    • cites [34] Mori TA Puddey IB Burke V Croft KD Dunstan DW Rivera JH Beilin LJ Effect of omega 3 fatty acids on oxidative stress in humans: GC-MS measurement of urinary F-2-isoprostane excretion Redox Report 2000 5 45 6 10905544 source

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    • cites [35] Nalsen C Vessby B Berglund L Uusitupa M Hermansen K Riccardi G Rivellese A Storlien L Erkkila A Yla-Herttuala S Tapsell L Basu S Dietary (n-3) fatty acids reduce plasma F-2-isoprostanes but not prostaglandin F-2 alpha in healthy humans J Nutr 2006 136 1222 8 16614408 source

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  • May combine two claims.

    Interpretationcitation

    Stress and depression promote less healthy food choices that can increase inflammation.

    “Thus, in general, stress and depression promote less healthy food choices that can boost inflammation.”
    Quote in the paperSubstantial claim0 of 5 sources checked
    • cites [42] Adam TC Epel ES Stress, eating and the reward system Physiology & Behavior 2007 91 449 58 17543357 source

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    • cites [43] Wardle J Steptoe A Oliver G Lipsey Z Stress, dietary restraint and food intake J Psychosom Res 2000 48 195 202 10719137 source

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    • cites [44] Liu C Xie B Chou CP Koprowski C Zhou D Palmer P Sun P Guo Q Duan L Sun X Anderson Johnson C Perceived stress, depression and food consumption frequency in the college students of China Seven Cities Physiol Behav 2007 92 748 54 17585967 source

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    • cites [45] Mikolajczyk RT El Ansari W Maxwell AE Food consumption frequency and perceived stress and depressive symptoms among students in three European countries Nutr J 2009 8 31 19604384 PMC2716364 source

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    • cites [46] Eng PM Kawachi I Fitzmaurice G Rimm EB Effects of marital transitions on changes in dietary and other health behaviours in US male health professionals J Epidemiol Community Health 2005 59 56 62 15598728 PMC1763358 source

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10 of 10

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Dietary intake and the microbiome are potent modulators of inflammatory pathways.

    “Finally, it is important to note that dietary intake and the microbiome are potent modulators of inflammatory pathways (Kiecolt-Glaser, 2010;Petra et al, 2015)”

    From Inflammation in Fear- and Anxiety-Based Disorders: PTSD, GAD, and Beyond (2017) · cites this paper as Kiecolt-Glaser, 2010

    The Abstract and ‘Diet and Inflammation’ section state that dietary components and dietary patterns influence inflammatory pathways. The discussion of bacterial endotoxins after high-fat meals does not establish that the microbiome itself modulates those pathways; the microbiome part of the claim is not supported by this paper. (LLM, conf=0.87)

    Experimental — accuracy not yet measured
  • Physical activity bolsters mediating immune proteins and gene expression and more distal biological aging endpoints, such as mitochondrial health and telomerase levels, which are related to telomere maintenance.

    “Physical activity also bolsters mediating immune proteins and gene expression (74,75) and more distal biological aging endpoints, such as mitochondrial health and telomerase levels (76–79), which are intimately related to telomere maintenance (20,80,81).”

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Authors
Kiecolt-Glaser, J. K.
Venue
Psychosomatic Medicine
Published
2010-05
Volume
72
Issue
4
Pages
365-369
ISSN
0033-3174 (ISSN-L)
OpenAlex
W1988667864
Cited by
310
References
62
Citations by year
2026: 10 · 2025: 17 · 2024: 17 · 2023: 18 · 2022: 23 · 2021: 15 · 2020: 65 · 2019: 16 · 2018: 22 · 2017: 18 · 2016: 13 · 2015: 9 · 2014: 13 · 2013: 19 · 2012: 23
FWCI
1.21
Type
journal article
Language
en
Open access
Locations
  • Psychosomatic Medicine (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institute on Aging (R01AG029562, AG029562)
  • National Cancer Institute (CA126857, R01CA126857, CA131029, R01CA131029)
  • National Center for Research Resources (UL1RR025755)
  • National Center for Complementary and Integrative Health (R21AT003912, AT003912)
Topics
  • Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
  • Life Sciences › Neuroscience › Neurology › Vagus Nerve Stimulation Research
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
Keywords
psychoneuroimmunology, inflammation, stress, diet, depression, vagus nerve, vagal tone, omega-3 fatty acids, NF-κB, oxidative stress, inflammatory cytokines, lipopolysaccharide response, gut-brain axis, food choice, mood
MeSH terms
C-Reactive Protein, Cause of Death, Diet, Eating, Fatty Acids, Unsaturated, Humans, Inflammation, Nutritional Physiological Phenomena, Psychoneuroimmunology, Stress, Psychological, Tumor Necrosis Factor-alpha, Fatty Acids, Omega-3

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